An endometriosis is a common disease in an obstetric and gynecologic field, and manifested in 10% of all females at an age capable of reproduction (non-patent reference 1). A tissues of an endometriosis leads via a periodic proliferation and degradation similarly to a eutopic endometrium to a periodic dysmenorrhea, dyspareunia, pelvic pain and menstrual erythrocyturia. In addition, 30 to 40% of infertility patients are reported to have such a disease (non-patent reference 2). While a mechanism by which an endometrial cell is migrated and then proliferated locally in some of the patients is still unknown, it is possible that the de-regulation of an inflammatory cytokine is responsible for the advancement of an endometriosis (non-patent reference 3, 4). In fact, activation and migration into a peritoneum of a monocyte is one of the immunological abnormalities reported most consistently in the endometriosis (non-patent references 5 to 8).
A dioxin is one of endocrine disturbing substances and exists ubiquitously in an environment. 3,3,7,8-Tetrachlorodibenzo-p-dioxisin (TCDD; dioxin) is a substance having a highest toxicity among the dioxins, and exhibits various toxic effects (for example, immunotoxicity, hematotoxicity, teratogenicity, oncogenicity and the like) (non-patent references 9, 10). A change in a gene expression induced by TCDD and related compounds is initiated at the time point of the binding of a toxin to an allyl hydrocarbon receptor (AhR), and then a dimer with an allyl hydrocarbon receptor nuclear translocator (ARNT) is formed and a complex capable of interacting with a gene regulation element containing an XRE (xenobiotic responsive element) motif (non-patent references 11, 12). Since when a monkey was exposed chronically to TCDD a mild to severe endometriosis was developed dose-dependently (non-patent reference 13), several studies have been made on the relationship between a dioxin and an endometriosis (non-patent references 14 to 18). On the other hand, a recent report taught that a TCDD exposure is not correlated with an endometriosis (non-patent references 19, 20), and the relationship between the dioxin exposure and the endometriosis still remains unclear.
Applicants have identified a TCDD target gene including an IgE-dependent histamine releasing factor (HRF) (non-patent references 21 to 23). Nevertheless, no relationship has been suggested been such an HRF as a TCDD target gene product and the endometriosis.    Non-patent reference 1: Wheeler J. M. J. Reprod Med. 1989, 34(1):41-6    Non-patent reference 2: Candiani G. B. et al., Obstct Gynecol. Surv. 1991, 46(6):374-82    Non-patent reference 3: Garcia-Velasco J. A. and Arici A. Fertil Steril. 1999, 71(6):983-93    Non-patent reference 4: Barcz et al., Med. Sci. Monit. 2000, 6(5):1042-6    Non-patent reference 5: Jolicoeur C. et al., Am. J. Pathol. 1998, 152(1): 125-33    Non-patent reference 6: Lebovic D. I. et al., Fertil Steril 2001, 75(1):1-10    Non-patent reference 7: Hornung D. et al., Am. J. Pathol. 2001, 158(6):1949-54    Non-patent reference 8: Blumenthal R. D. et al., Am. J. Pathol. 2000, 156(5): 1581-8    Non-patent reference 9: Chapman D. E. and Schiller C. M. Toxicol Appl. Pharmacol. 1985, 78(1):147-57    Non-patent reference 10: McGregor D. B. et al., Environ Health Perspect. 1998, 106 Suppl. 2:755-60    Non-patent reference 11: Sagawa K. and Fujii-Kuriyama T. J. Biochem. (Tokyo) 1997, 122(6):1075-9    Non-patent reference 12: Nebert D. W. Crit. Rev. Toxicol. 1989, 20(3):153-74    Non-patent reference 13: Rier S. E. et al., Fundam. Appl. Toxicol. 1993, 21(4):433-41    Non-patent reference 14: Gibbsons A. Science 1993, 262(5183): 1373    Non-patent reference 15: Obsteen K. G. and Sierra-Rivera E. Endocrinol. 1997, 15(3):301-8    Non-patent reference 16: Bruner-Tran K. L. et al. Gynecol. Obstet. Invest. 1999, 48 Suppl. 1:45-56    Non-patent reference 17: Johson K. L. et al., Environ Health Perspect 1997, 105(7):750-5    Non-patent reference 18: Yang J. Z. and Foster W. G. Toxicol. Ind. Health 1997, 13(1):15-25    Non-patent reference 19: Igarashi T. et al., Endocr. J. 1999, 46(6):765-72    Non-patent reference 20: Pauwels A. et al., Hum. Reprod. 2001, 16(10):2050-5    Non-patent reference 21: Oikawa K. et al., Cancer Res. 2001, 61(15):5707-9    Non-patent reference 22: Oikawa K. et al., Biochem. Biophys. Res. Commun. 2002, 290(3):984-7    Non-patent reference 23: Ohbayashi et al., FEBS Lett. 2001, 508(3):341-4